Mellwig Klaus P, van Buuren Frank, Schmidt Henning K, Wielepp Peter, Burchert Wolfgang, Horstkotte Dieter
Department of Cardiology, Nuclear Medicine and Molecular Imaging, Heart Center North Rhine-Westphalia, Bad Oeynhausen, Germany.
Ther Apher Dial. 2006 Dec;10(6):510-7. doi: 10.1111/j.1744-9987.2006.00441.x.
Hypercholesterolemia impairs endothelial function and subsequently decreases coronary vasodilatatory capacity. We examined the quantitative effects of one single LDL apheresis on vasodilatatory capacity. Using N-13 ammonia as a tracer for dynamic quantitative positron emission tomography (PET), mean myocardial perfusion measurements were carried out before and 20 h later after LDL apheresis, both under resting conditions and after pharmacological vasodilatation with dipyridamole. LDL apheresis was carried out using the heparin induced extracorporeal LDL precipitation (H.E.L.P.) procedure. We examined 47 patients (12 women and 35 men), with angiographically-proven coronary artery disease. All of them suffered from hypercholesterolemia. Of the patients, 35 received a chronic weekly H.E.L.P. procedure (group A), while H.E.L.P. procedure treatment was started for the first time in 12 patients, who were subsequently enrolled in a chronic apheresis program (group B). H.E.L.P. apheresis was combined with cholesterol lowering drugs in all patients. Both groups underwent positron emission tomography twice (prior to LDL apheresis and 20 h later). In group A, LDL cholesterol levels decreased from 175 +/- 50 mg/dL to 60 +/- 21 mg/dL immediately after H.E.L.P. (77 +/- 25 mg/dL before the second PET). Corresponding values for fibrinogen levels were 287 +/- 75 mg/dL to 102 +/- 29 mg/dL (155 +/- 52 mg/dL), minimal coronary resistance dropped from 0.56 +/- 0.20 to 0.44 +/- 0.17 mm Hg x 100 g x min/mL (P < 0.0001). Plasma viscosity decreased by 7.8%. In group B, LDL cholesterol decreased from 187 +/- 45 mg/dL to 75 +/- 27 mg/dL (85 +/- 29 mg/dL) and fibrinogen from 348 +/- 65 mg/dL to 126 +/- 38 mg/dL (168 +/- 45 mg/dL). Minimal coronary resistance was reduced from 0.61 +/- 0.23 to 0.53 +/- 0.19 mm Hg x 100 g x min/mL (P < 0.01). Plasma viscosity was observed to decrease by 7.6%. The strong LDL drop in patients under chronic H.E.L.P. treatment has a significant impact on coronary vasodilatatory capacity within 20 h leading to an improved overall cardiac perfusion. Nearly the same effect can be seen in patients after their first H.E.L.P. treatment.
高胆固醇血症会损害内皮功能，进而降低冠状动脉扩张能力。我们研究了单次低密度脂蛋白（LDL）血液成分分离术对血管扩张能力的定量影响。使用N - 13氨作为动态定量正电子发射断层扫描（PET）的示踪剂，在LDL血液成分分离术前和术后20小时，分别在静息状态下以及用双嘧达莫进行药物性血管扩张后，进行平均心肌灌注测量。LDL血液成分分离术采用肝素诱导的体外LDL沉淀（H.E.L.P.）程序。我们研究了47例经血管造影证实患有冠状动脉疾病的患者（12名女性和35名男性）。他们均患有高胆固醇血症。其中35例患者接受每周一次的慢性H.E.L.P.程序治疗（A组），而12例患者首次开始接受H.E.L.P.程序治疗，随后纳入慢性血液成分分离术项目（B组）。所有患者的H.E.L.P.血液成分分离术均与降胆固醇药物联合使用。两组患者均接受两次正电子发射断层扫描（LDL血液成分分离术前和术后20小时）。在A组中，H.E.L.P.治疗后立即，LDL胆固醇水平从175±50mg/dL降至60±21mg/dL（第二次PET检查前为77±25mg/dL）。纤维蛋白原水平的相应值为287±75mg/dL至102±29mg/dL（155±52mg/dL），最小冠状动脉阻力从0.56±0.20降至0.44±0.17mmHg×100g×min/mL（P<0.0001）。血浆粘度下降了7.8%。在B组中，LDL胆固醇从187±45mg/dL降至75±27mg/dL（85±29mg/dL），纤维蛋白原从348±65mg/dL降至126±38mg/dL（168±45mg/dL）。最小冠状动脉阻力从0.61±0.23降至0.53±0.19mmHg×100g×min/mL（P<0.01）。观察到血浆粘度下降了7.6%。接受慢性H.E.L.P.治疗的患者中LDL的大幅下降在20小时内对冠状动脉扩张能力有显著影响，导致整体心脏灌注得到改善。首次接受H.E.L.P.治疗的患者也能看到几乎相同的效果。
